Clinical and neurobiological effects of aerobic endurance training in multi-episode schizophrenia patients

2016 ◽  
Vol 33 (S1) ◽  
pp. S41-S41
Author(s):  
P. Falkai
Keyword(s):  
Aerobic Exercise ◽  
Neural Plasticity ◽  
Neural Progenitor Cells ◽  
Hippocampal Volume ◽  
Brain Disorder ◽  
Healthy Humans ◽  
Proliferation And Differentiation ◽  
Competing Interest ◽  
Related Proteins ◽  
The Brain

Schizophrenia is a severe brain disorder characterised by positive, negative, affective and cognitive symptoms and can be viewed as a disorder of impaired neural plasticity. Aerobic exercise has a profound impact on the plasticity of the brain of both rodents and humans such as inducing the proliferation and differentiation of neural progenitor cells of the hippocampus in mice and rats. Aerobic exercise enhances LTP and leads to a better performance in hippocampus related memory tasks, eventually by increasing metabolic and synaptic plasticity related proteins in the hippocampus. In healthy humans, regular aerobic exercise increases hippocampal volume and seems to diminish processes of ageing like brain atrophy and cognitive decline.Disclosure of interestThe author has not supplied his declaration of competing interest.

From Identification of Neurofunctional Systems to Individualization of Treatment for Schizophrenic Disorders

2017 ◽  
Vol 41 (S1) ◽  
pp. S52-S52
Author(s):  
P. Falkai
Keyword(s):  
Neural Plasticity ◽  
Partial Recovery ◽  
Imaging Data ◽  
Brain Disorder ◽  
Residual Symptoms ◽  
Intermediate Group ◽  
Outcome Group ◽  
Targeted Treatments ◽  
Competing Interest ◽  
Long Term Prognosis

Schizophrenia is a severe brain disorder characterized by positive, negative, affective and cognitive symptoms and can be viewed as a disorder of impaired neural plasticity. Schizophrenia leads to livelong disability in a substantial proportion of the sufferers and it still connected with an unfavorable outcome. Therefore, it is inevitable to find and apply interventions to reduce the risk of psychosis and/or prevent a further chronification of the illness. There are two major obstacles translational schizophrenia research has to face: One is the introduction of easy to measure and reliable biomarkers; the second are add-on treatments to improve the residual symptoms of this illness. To reach the first goal, subgroups must be identified utilizing biomarkers in order to induce specifically targeted treatments. For the long-term prognosis and outcome it is necessary for biomarkers to constitute easy measurable clinical routine parameters. Studies will be summarized using clinical (GAF, PANSS, CGI) and imaging data in order to accurately predict the outcome in the first week, for 4 and for 52 weeks. This will help to subdivide these groups into a god, an intermediate and a fair outcome group. Future clinical studies will benefit enormously if it was possible to focus on the intermediate group, where recovery could be reached by targeted treatment as most of those subjects are showing partial recovery or remission.Disclosure of interestThe author declares that he has no competing interest.

scholarly journals The unbalanced reorganization of weaker functional connections induces the altered brain network topology in schizophrenia

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rossana Mastrandrea ◽  
Fabrizio Piras ◽  
Andrea Gabrielli ◽  
Nerisa Banaj ◽  
Guido Caldarelli ◽  
...  
Keyword(s):  
Resting State ◽  
Functional Organization ◽  
Functional Integration ◽  
Brain Network ◽  
Modular Organization ◽  
Node Degree ◽  
Imaging Data ◽  
Brain Disorder ◽  
Functional Connections ◽  
The Brain

AbstractNetwork neuroscience shed some light on the functional and structural modifications occurring to the brain associated with the phenomenology of schizophrenia. In particular, resting-state functional networks have helped our understanding of the illness by highlighting the global and local alterations within the cerebral organization. We investigated the robustness of the brain functional architecture in 44 medicated schizophrenic patients and 40 healthy comparators through an advanced network analysis of resting-state functional magnetic resonance imaging data. The networks in patients showed more resistance to disconnection than in healthy controls, with an evident discrepancy between the two groups in the node degree distribution computed along a percolation process. Despite a substantial similarity of the basal functional organization between the two groups, the expected hierarchy of healthy brains' modular organization is crumbled in schizophrenia, showing a peculiar arrangement of the functional connections, characterized by several topologically equivalent backbones. Thus, the manifold nature of the functional organization’s basal scheme, together with its altered hierarchical modularity, may be crucial in the pathogenesis of schizophrenia. This result fits the disconnection hypothesis that describes schizophrenia as a brain disorder characterized by an abnormal functional integration among brain regions.

scholarly journals Ecklonia cava Attenuates PM2.5-Induced Cognitive Decline through Mitochondrial Activation and Anti-Inflammatory Effect

Marine Drugs ◽  
2021 ◽  
Vol 19 (3) ◽  
pp. 131
Author(s):  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Jong Min Kim ◽  
Hyun-Jin Kim ◽  
Ho Jin Heo
Keyword(s):  
Water Extract ◽  
Ecklonia Cava ◽  
Mitochondrial Activity ◽  
Memory Decline ◽  
Mitochondria Membrane Potential ◽  
Mitochondrial Ros ◽  
Ifn Γ ◽  
Related Proteins ◽  
The Brain ◽  
Pro Inflammatory Cytokines

To evaluate the effects of Ecklonia cava (E. cava) on ambient-pollution-induced neurotoxicity, we used a mouse model exposed to particulate matter smaller than 2.5 µm in aerodynamic diameter (PM2.5). The intake of water extract from E. cava (WEE) effectively prevented the learning and memory decline. After a behavioral test, the toll-like receptor (TLR)-4-initiated inflammatory response was confirmed by PM2.5 exposure in the lung and brain tissues, and the WEE was regulated through the inhibition of nuclear factor-kappa B (NF-κB)/inflammasome formation signaling pathway and pro-inflammatory cytokines (IL-6 and IFN-γ). The WEE also effectively improved the PM2.5-induced oxidative damage of the lungs and brain through the inhibition of malondialdehyde (MDA) production and the activation of mitochondrial activity (mitochondrial ROS content, mitochondria membrane potential (MMP), adenosine triphosphate (ATP) content, and mitochondria-mediated apoptotic molecules). In particular, the WEE regulated the cognition-related proteins (a decreased amyloid precursor protein (APP) and p-Tau, and an increased brain-derived neurotrophic factor (BDNF)) associated with PM2.5-induced cognitive dysfunction. Additionally, the WEE prevented the inactivation of acetylcholine (ACh) synthesis and release as a neurotransmitter by regulating the acetylcholinesterase (AChE) activity, choline acetyltransferase (ChAT), and ACh receptor (AChR)-α3 in the brain tissue. The bioactive compounds of the WEE were detected as the polysaccharide (average Mw; 160.13 kDa) and phenolic compounds including 2′-phloroeckol.

Nicotine as therapeutic agent in treatment of mood disorders

2016 ◽  
Vol 33 (S1) ◽  
pp. S552-S552
Author(s):  
C. Tsopelas ◽  
N. Petros ◽  
D. Maria ◽  
P. Dimitris ◽  
G.G. Angelica ◽  
...  
Keyword(s):  
Mood Disorders ◽  
Acetylcholine Receptors ◽  
Web Search ◽  
Therapeutic Agent ◽  
Negative Attitude ◽  
Medical Databases ◽  
Positive Effects ◽  
Complex Interactions ◽  
Competing Interest ◽  
The Brain

IntroductionThe plant that has as active ingredient nicotine was chewed or smoked for many years from American natives, for its therapeutic properties. Nowadays after the extensive negative attitude towards smoking, the main provider of nicotine, researchers are now pointing out the therapeutic possibilities of nicotine in mood disorders, as a substance that is acting in the acetylcholine receptors in the brain.AimsIn this review we are trying to explore the possibilities of nicotine use as a therapeutic agent.MethodsWe did a detailed research of the main medical databases, and web search engines for relevant studies. We scrutinize them independently, before reaching consensus about appropriateness for inclusion in the study.ResultsDiadermal administration of nicotine has a positive effect in depressive disorder in 3–8 days, an effect that in one study was reversed after cessation of nicotine. Patients with depression and/or healthy subjects show improvement of attention and working memory after diadermal use of nicotine. Research is not conclusive in the sustainability of these positive affects as other researchers emphasize their short effect in mood.ConclusionNicotine presents as part of novel and promising therapeutic agents with complex interactions with other neurotransmitters in the brain. Before condemning nicotine along with smoking we should acknowledge the potential use of nicotine as a therapeutic compound since research shows that some of these positive effects appear not only to smokers after abstinence but also to non-smokers.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Neural Progenitor Cells Undergoing Yap/Tead-Mediated Enhanced Self-Renewal Form Heterotopias More Easily in the Diencephalon than in the Telencephalon

2018 ◽  
Vol 43 (1) ◽  
pp. 180-189 ◽  
Author(s):  
Kanako Saito ◽  
Ryotaro Kawasoe ◽  
Hiroshi Sasaki ◽  
Ayano Kawaguchi ◽  
Takaki Miyata
Keyword(s):  
Progenitor Cells ◽  
Neural Tube ◽  
Neural Progenitor Cells ◽  
Three Dimensional ◽  
Neural Progenitor ◽  
Hippo Signaling ◽  
Apical Surface ◽  
Elevated Expression ◽  
Underlying Mechanisms ◽  
The Brain

Abstract Spatiotemporally ordered production of cells is essential for brain development. Normally, most undifferentiated neural progenitor cells (NPCs) face the apical (ventricular) surface of embryonic brain walls. Pathological detachment of NPCs from the apical surface and their invasion of outer neuronal territories, i.e., formation of NPC heterotopias, can disrupt the overall structure of the brain. Although NPC heterotopias have previously been observed in a variety of experimental contexts, the underlying mechanisms remain largely unknown. Yes-associated protein 1 (Yap1) and the TEA domain (Tead) proteins, which act downstream of Hippo signaling, enhance the stem-like characteristics of NPCs. Elevated expression of Yap1 or Tead in the neural tube (future spinal cord) induces massive NPC heterotopias, but Yap/Tead-induced expansion of NPCs in the developing brain has not been previously reported to produce NPC heterotopias. To determine whether NPC heterotopias occur in a regionally characteristic manner, we introduced the Yap1-S112A or Tead-VP16 into NPCs of the telencephalon and diencephalon, two neighboring but distinct forebrain regions, of embryonic day 10 mice by in utero electroporation, and compared NPC heterotopia formation. Although NPCs in both regions exhibited enhanced stem-like behaviors, heterotopias were larger and more frequent in the diencephalon than in the telencephalon. This result, the first example of Yap/Tead-induced NPC heterotopia in the forebrain, reveals that Yap/Tead-induced NPC heterotopia is not specific to the neural tube, and also suggests that this phenomenon depends on regional factors such as the three-dimensional geometry and assembly of these cells.

scholarly journals Regeneration, Plasticity, and Induced Molecular Programs in Adult Zebrafish Brain

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Mehmet Ilyas Cosacak ◽  
Christos Papadimitriou ◽  
Caghan Kizil
Keyword(s):  
Neural Plasticity ◽  
Molecular Mechanisms ◽  
Clinical Settings ◽  
Regenerative Capacity ◽  
Zebrafish Brain ◽  
Aquatic Vertebrates ◽  
Neural Stem Progenitor Cells ◽  
Set Up ◽  
Regenerative Therapies ◽  
The Brain

Regenerative capacity of the brain is a variable trait within animals. Aquatic vertebrates such as zebrafish have widespread ability to renew their brains upon damage, while mammals have—if not none—very limited overall regenerative competence. Underlying cause of such a disparity is not fully evident; however, one of the reasons could be activation of peculiar molecular programs, which might have specific roles after injury or damage, by the organisms that regenerate. If this hypothesis is correct, then there must be genes and pathways that (a) are expressed only after injury or damage in tissues, (b) are biologically and functionally relevant to restoration of neural tissue, and (c) are not detected in regenerating organisms. Presence of such programs might circumvent the initial detrimental effects of the damage and subsequently set up the stage for tissue redevelopment to take place by modulating the plasticity of the neural stem/progenitor cells. Additionally, if transferable, those “molecular mechanisms of regeneration” could open up new avenues for regenerative therapies of humans in clinical settings. This review focuses on the recent studies addressing injury/damage-induced molecular programs in zebrafish brain, underscoring the possibility of the presence of genes that could be used as biomarkers of neural plasticity and regeneration.

Differential energetic response of brain vs. skeletal muscle upon glycemic variations in healthy humans

2008 ◽  
Vol 294 (1) ◽  
pp. R12-R16 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Uwe H. Melchert ◽  
Harald G. Scholand-Engler ◽  
Maria C. Howitz ◽  
Bernd Schultes ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Underlying Mechanism ◽  
High Energy ◽  
Resonance Spectroscopy ◽  
Energy Status ◽  
High Energy Phosphate ◽  
Available Energy ◽  
Healthy Humans ◽  
High Energy Phosphate Metabolism ◽  
The Brain

The brain regulates all metabolic processes within the organism, and therefore, its energy supply is preserved even during fasting. However, the underlying mechanism is unknown. Here, it is shown, using 31P-magnetic resonance spectroscopy that during short periods of hypoglycemia and hyperglycemia, the brain can rapidly increase its high-energy phosphate content, whereas there is no change in skeletal muscle. We investigated the key metabolites of high-energy phosphate metabolism as rapidly available energy stores by 31P MRS in brain and skeletal muscle of 17 healthy men. Measurements were performed at baseline and during dextrose or insulin-induced hyperglycemia and hypoglycemia. During hyperglycemia, phosphocreatine (PCr) concentrations increased significantly in the brain ( P = 0.013), while there was a similar trend in the hypopglycemic condition ( P = 0.055). Skeletal muscle content remained constant in both conditions ( P > 0.1). ANOVA analyses comparing changes from baseline to the respective glycemic plateau in brain (up to +15%) vs. muscle (up to −4%) revealed clear divergent effects in both conditions ( P < 0.05). These effects were reflected by PCr/Pi ratio ( P < 0.05). Total ATP concentrations revealed the observed divergency only during hyperglycemia ( P = 0.018). These data suggest that the brain, in contrast to peripheral organs, can activate some specific mechanisms to modulate its energy status during variations in glucose supply. A disturbance of these mechanisms may have far-reaching implications for metabolic dysregulation associated with obesity or diabetes mellitus.

Converging Evidence That Neural Plasticity Underlies Transcranial Direct-Current Stimulation

2021 ◽  
Vol 33 (1) ◽  
pp. 146-157
Author(s):  
Chong Zhao ◽  
Geoffrey F. Woodman
Keyword(s):  
Visual Search ◽  
Direct Current ◽  
Neural Plasticity ◽  
Transcranial Direct Current Stimulation ◽  
Time Course ◽  
Memory Task ◽  
Long Term Memory ◽  
Visual Stream ◽  
Direct Current Stimulation ◽  
The Brain

It is not definitely known how direct-current stimulation causes its long-lasting effects. Here, we tested the hypothesis that the long time course of transcranial direct-current stimulation (tDCS) is because of the electrical field increasing the plasticity of the brain tissue. If this is the case, then we should see tDCS effects when humans need to encode information into long-term memory, but not at other times. We tested this hypothesis by delivering tDCS to the ventral visual stream of human participants during different tasks (i.e., recognition memory vs. visual search) and at different times during a memory task. We found that tDCS improved memory encoding, and the neural correlates thereof, but not retrieval. We also found that tDCS did not change the efficiency of information processing during visual search for a certain target object, a task that does not require the formation of new connections in the brain but instead relies on attention and object recognition mechanisms. Thus, our findings support the hypothesis that direct-current stimulation modulates brain activity by changing the underlying plasticity of the tissue.

scholarly journals THE VISUAL SYSTEM: A "CHICKEN AND EGG" PROBLEM SOLVED

2009 ◽  
Vol 05 (01) ◽  
pp. 115-121
Author(s):  
ANDREW R. PARKER ◽  
H. JOHN CAULFIELD
Keyword(s):  
Visual System ◽  
Neural Plasticity ◽  
Neural Circuit ◽  
Process Data ◽  
System A ◽  
New Information ◽  
The Brain

"What comes first: the chicken or the egg?" Eyes and vision were a great concern for Darwin. Recently, religious fundamentalists have started to attack evolution on the grounds that this is a chicken and egg problem. How could eyes improve without the brain module to use the new information that eye provides? But how could the brain evolve a neural circuit to process data not available to it until a new eye capability emerges? We argue that neural plasticity in the brain allows it to make use of essentially any useful information the eye can produce. And it does so easily within the animal's lifetime. Richard Gregory suggested something like this 40 years ago. Our work resolves a problem with his otherwise-insightful work.

Sign in / Sign up

Export Citation Format

Share Document